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Melatonin attenuates lung ischemia-reperfusion injury through SIRT3 signaling-dependent mitophagy in type 2 diabetic rats.
Song, Zhiqiang; Yan, Congmin; Zhan, Yuanbo; Wang, Qiujun; Zhang, Yina; Jiang, Tao.
Affiliation
  • Song Z; Department of Geriatrics, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
  • Yan C; Department of Anesthesiology (Hei Long Jiang Province Key Lab of Research on Anesthesiology and Critical Care Medicine), The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
  • Zhan Y; Department of Periodontology and Oral Mucosa, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
  • Wang Q; Department of General Practice, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
  • Zhang Y; Department of Geriatrics, The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
  • Jiang T; Department of Anesthesiology (Hei Long Jiang Province Key Lab of Research on Anesthesiology and Critical Care Medicine), The Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Exp Lung Res ; 49(1): 101-115, 2023.
Article in En | MEDLINE | ID: mdl-37265380
ABSTRACT

Background:

Lung ischemia-reperfusion injury (LIRI) remains the major cause of primary lung dysfunction after lung transplantation. Diabetes mellitus (DM) is an independent risk factor for morbidity and mortality following lung transplantation. Mitochondrial dysfunction is recognized as a key mediator in the pathogenesis of diabetic LIRI. Melatonin has been reported to be a safe and potent preserving mitochondrial function agent. This study aimed at investigating the potential therapeutic effect and mechanisms of melatonin on diabetic LIRI.

Methods:

High-fat-diet-fed streptozotocin-induced type 2 diabetic rats were exposed to melatonin, with or without administration of the SIRT3 short hairpin ribonucleic acid (shRNA) plasmid following a surgical model of ischemia-reperfusion injury of the lung. Lung function, inflammation, oxidative stress, cell apoptosis, and mitochondrial function were examined.

Results:

The SIRT3 signaling and mitophagy were suppressed following diabetic LIRI. Treatment with melatonin markedly induced mitophagy and restored SIRT3 expression. Melatonin treatment also attenuated subsequent diabetic LIRI by improving lung functional recovery, suppressing inflammation, decreasing oxidative damage, diminishing cell apoptosis, and preserving mitochondrial function. However, either administration of SIRT3 shRNA or an autophagy antagonist 3-methyladenine (3-MA) suppressing mitophagy, and compromised the protective action of melatonin.

Conclusion:

Data indicated that melatonin attenuates diabetic LIRI through activation of SIRT3 signaling-mediated mitophagy.
Subject(s)
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Reperfusion Injury / Diabetes Mellitus, Experimental / Diabetes Mellitus, Type 2 / Sirtuin 3 / Melatonin Type of study: Prognostic_studies / Risk_factors_studies Limits: Animals Language: En Journal: Exp Lung Res Year: 2023 Document type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Reperfusion Injury / Diabetes Mellitus, Experimental / Diabetes Mellitus, Type 2 / Sirtuin 3 / Melatonin Type of study: Prognostic_studies / Risk_factors_studies Limits: Animals Language: En Journal: Exp Lung Res Year: 2023 Document type: Article Affiliation country: China
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